There is No 'Silver Bullet' to Reducing Obesity Risk

Many fattening aspects of the environment, lifestyle and
behavior interact with a person's genes to influence his or her
waistline - and that the strongest influence is from poverty, revealed a new study led by the University of Exeter Medical School.

The findings contradict some studies, which have concluded that
concentrating obesity policy on specific aspects such as the consumption
of fizzy drinks or fried food could make a meaningful difference to
help decrease waistlines, especially in those of us at high genetic risk
of obesity.

The new research challenges this, and concludes that it is
premature to suggest that specific aspects of behavior or the
environment can be targeted to reduce obesity levels effectively in
people at high risk due to their genes.

‘People experiencing less favorable socioeconomic circumstances and at high genetic risk were overweight to a greater extent than would be expected by simply adding up the two risk factors.’

Dr. Jessica Tyrrell, who led the research, said: "Our findings suggest
that it is premature to target any particular aspect of the environment
or behavior to try to reduce obesity. There is no 'silver bullet' to
reducing obesity risk. It is misleading to suggest public health
measures should be targeted specifically at fried food reduction, fizzy
drink consumption or TV watching in those genetically predisposed to
obesity, as some previous studies in leading medical journals have
suggested. Instead, the data are consistent with proposals that public
health measures should aim to alter all aspects of these fattening
factors in small ways to have more impact in lowering levels of obesity
and type 2 diabetes."

A person's genes can mean they are more susceptible to becoming obese
or developing type 2 diabetes in today's modern world of plentiful food
and sedentary lifestyles. However, until now, little has been known
about how genes interact with the modern environment and human behavior
to mean some people with this predisposition become obese, while others
remain slim.

The study, published in the International Journal of Epidemiology,
used 120,000 individuals from the UK Biobank, and could influence
future policy on reducing obesity, one of today's greatest global health
challenges. In the UK, obesity affects around one in every four adults
and one in every five children aged 10-11, according to the NHS. Being
obese increases risk of developing type 2 diabetes, coronary heart
disease, some cancers and stroke.

The study concludes that poverty is likely to be related to many
different factors, reflecting socioeconomic influences on diet and
activity levels. Previous studies have shown that in high income
countries people from more deprived social backgrounds are more likely
to be obese, but this study provides the strongest evidence yet that
these effects are even stronger in people at the highest genetic risk of
obesity. This type of study was not possible until recently, when large
numbers of genetic variants altering BMI, a measure of weight, were
discovered.

The team found the first robust evidence that people experiencing
less favorable socioeconomic circumstances and at high genetic risk
were overweight to a greater extent than would be expected by simply
adding up the two risk factors. The differences do not push people from
normal weight to obesity but add a few kilograms of weight - enough to
make an important additional contribution to the strain placed on
healthcare systems.

The authors found that, within the poorest half of the population,
carrying 10 additional genetic risk factors for obesity was associated
with approximately 3.8kg extra weight in someone 1.73m tall. In
contrast, being of the same height and carrying the same number of
obesity risk genetic factors was associated with just 2.9kg extra weight
in the richest half of the population.

Professor Tim Frayling, of the University of Exeter Medical School,
oversaw the study. He said: "In order to inform evidence-based policy
decisions around obesity, we need to understand more about the complex
mix of genes, environment, behaviour and lifestyle. Our study suggests
that genes and environment can interact to provide a "double whammy"
type effect, but, critically, it is really hard to narrow down which
parts of the environment and lifestyle are the most critical. Large
genetic datasets from resources like the UK Biobank are helping us pick
the problem apart."

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